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Research Project: Intervention Strategies to Control and Eradicate Foreign Animal Diseases of Swine

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Title: Evaluation of the deletion of African swine fever virus E111R gene from the Georgia isolate in virus replication and virulence in domestic pigs

Author
item Ramirez Medina, Elizabeth
item Velazquez Salinas, Lauro
item VALLADARES, ALYSSA - Oak Ridge Institute For Science And Education (ORISE)
item Silva, Ediane
item Burton, Leeanna
item Clark, Jason
item Borca, Manuel
item Gladue, Douglas

Submitted to: Viruses
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/18/2024
Publication Date: 9/23/2024
Citation: Ramirez Medina, E., Velazquez Salinas, L., Valladares, A., Silva, E.B., Burton, L.J., Clark, J.A., Borca, M.V., Gladue, D.P. 2024. Evaluation of the deletion of African swine fever virus E111R gene from the Georgia isolate in virus replication and virulence in domestic pigs. Viruses. 16(9). Article 1502. https://doi.org/10.3390/v16091502.
DOI: https://doi.org/10.3390/v16091502

Interpretive Summary: African swine fever virus (ASFV) is the causative agent for African swine fever, a large virus with over 180 different open reading frames, where it is unknown if the encoding gene is essential for ASFV growth in cell culture or for pathogenesis. Here we investigated one of those genes, E111R, by deleting it from the ASFV genome, and concluded that there was no change in virus growth in cell culture or virus pathogenesis.

Technical Abstract: African swine fever virus (ASFV) is the causative agent of an often-lethal disease of domestic pigs, African swine fever (ASF). ASF is currently a pandemic disease challenging pig production in Eurasia. While ASFV genome encodes for over 160 proteins, the function of most of them are still not characterized. Among those ASF genes with un-known function is E111R gene. It has been recently reported that deletion of E111R gene from the genome of the virulent Chinese field isolate SY18 strain produced a reduction of virus virulence when inoculated at a relatively low dose. Conversely, we report here that deletion of the ASFV gene E111R in the Georgia 2010 isolate does not alter the virulence of the parental virus in experimentally inoculated pigs. A recombinant virus lacking the E111R gene, ASFV-G-deltaE111R was intramuscularly (IM) inoculated in domestic pigs at a dose of 102 HAD50 of ASFV-G-deltaE111R, and compared with animals that received a similar dose of virulent ASFV-G. Both animals inoculated with either the recombinant ASFV-G-deltaE111R or the parental virus developed a fatal form of the disease being euthanized around the 6th-7th day post inoculation.